Biomedical subjects

S Colman

Publications and source records attributed to S Colman.

5 recordsLinked to original sources

PubMed2001

BFIT, a unique acyl-CoA thioesterase induced in thermogenic brown adipose tissue: cloning, organization of the human gene and assessment of a potential link to obesity.

We hypothesized that certain proteins encoded by temperature-responsive genes in brown adipose tissue (BAT) contribute to the remarkable metabolic shifts observed in this tissue, thus prompting a differential mRNA expression analysis to identify candidates involved in this process in mouse BAT. An mRNA species corresponding to a novel partial-length gene was found to be induced 2-3-fold above the control following cold exposure (4 degrees C), and repressed approximately 70% by warm acclimation (33 degrees C, 3 weeks) compared with controls (22 degrees C). The gene displayed robust BAT expression (i.e. approximately 7-100-fold higher than other tissues in controls). The full-length murine gene encodes a 594 amino acid ( approximately 67 kDa) open reading frame with significant homology to the human hypothetical acyl-CoA thioesterase KIAA0707. Based on cold-inducibility of the gene and the presence of two acyl-CoA thioesterase domains, we termed the protein brown-fat-inducible thioesterase (BFIT). Subsequent analyses and cloning efforts revealed the presence of a novel splice variant in humans (termed hBFIT2), encoding the orthologue to the murine BAT gene. BFIT was mapped to syntenic regions of chromosomes 1 (human) and 4 (mouse) associated with body fatness and diet-induced obesity, potentially linking a deficit of BFIT activity with exacerbation of these traits. Consistent with this notion, BFIT mRNA was significantly higher ( approximately 1.6-2-fold) in the BAT of obesity-resistant compared with obesity-prone mice fed a high-fat diet, and was 2.5-fold higher in controls compared with ob/ob mice. Its strong, cold-inducible BAT expression in mice suggests that BFIT supports the transition of this tissue towards increased metabolic activity, probably through alteration of intracellular fatty acyl-CoA concentration.

Adipose Tissue↗

PubMed2000

Does HIV reporting by name deter testing? MESH Study Group.

OBJECTIVE: Name-based HIV reporting is controversial in the United States because of concerns that it may deter high-risk persons from being tested. We sought to determine whether persons at risk of HIV infection knew their state's HIV reporting policy and whether they had delayed or avoided testing because of it. DESIGN: A cross-sectional anonymous survey. METHODS: We interviewed 2404 participants in one of three high-risk groups: men who have sex with men (MSM), heterosexuals attending a sexually transmitted disease (STD) clinic, and street-recruited injection drug users (IDU). Participants were asked standardized questions about their knowledge of reporting policies and reasons for having delayed or avoided testing. We recruited in eight US states: four with name-based reporting and four without; all offered anonymous testing at certain sites. RESULTS: Fewer than 25% correctly identified their state's HIV reporting policy. Over 50% stated they did not know whether their state used name-based reporting. Of the total, 480 participants (20%) had never been tested. Of these, 17% from states with name-based reporting selected concern about reporting as a reason for not testing compared with 14% from states without name-based reporting (P = 0.5). Comparing previously tested participants from states with name-based reporting to those from states without, concern about HIV reporting was given as a reason for delaying testing by 26% compared with 13% of IDU (P < 0.001), and for 26% compared with 19% of MSM (P = 0.06). CONCLUSION: Most participants did not know their state's HIV reporting policy. Name-based reporting policies were not associated with avoiding HIV testing because of worry about reporting, although they may have contributed to delays in testing among some IDU.

AIDS Serodiagnosis↗

PubMed1996

Correlation of trisomy 12 with proliferating cells by combined immunocytochemistry and fluorescence in situ hybridization in chronic lymphocytic leukemia.

Conventional G-banding and fluorescence in situ hybridization (FISH) were performed on peripheral blood samples of 340 consecutive untreated cases of chronic lymphocytic leukemia (CLL) for the detection of trisomy 12 and other chromosome abnormalities. These findings were correlated with the proliferative activity of CLL lymphocytes assessed by the monoclonal antibody Ki-67. Cytogenetic analysis displayed a normal karyotype in 131 (38.5%) cases, trisomy 12 in 68 (20%), 31 by G-banding and an additional 37 cases by FISH, other clonal abnormalities in 47 (14%), and no metaphases in 94 (27.5%). The percentage of Ki-67-positive cells was significantly higher in cases with trisomy 12 (4.1 +/- 4.48) than in cases with a normal karyotype (1.5 +/- 2.0), those with other clonal abnormalities (1.35 +/- 1.37) and cases with no metaphases (1.14 +/- 1.6) (P< 0.0001). Cases with trisomy 12 were associated with more advanced clinical stage, atypical morphology and a higher percentage of Ki-67+ve cells than cases lacking trisomy 12 (P< 0.0001). Although there was no direct correlation between the percentage of trisomic and proliferating cells, the combination of immunocytochemistry and FISH showed that most Ki-67-positive cells were trisomic for chromosome 12. Our results suggest that the association of trisomy 12 with a higher proliferative activity supports the view that this abnormality is a secondary event associated with disease progression in CLL.

Adult↗

PubMed1993

Inhibition of HIV infection by flavanoids.

Of a variety of flavanoids, the flavans were generally more effective than flavones and flavanones in selective inhibition of HIV-1, HIV-2 or SIV infection. Studies of their effects on the binding of sCD4 and antibody to gp120 indicated that the effective compounds interact irreversibly with gp120 to inactive virus infectivity and block infection.

CD4 Antigens↗

PubMed1987

Chromosome aberrations and sister chromatid exchanges in Chinese hamster ovary cells: evaluations of 108 chemicals.

Results from the testing of 108 coded chemicals in Chinese hamster ovary (CHO) cells for the induction of chromosome aberrations and sister chromatid exchanges (SCEs) are presented. All chemicals were tested with and without exogenous metabolic activation, using protocols designed to allow testing up to toxic doses. Cell harvest times could also be extended if chemical-induced cell cycle delay was seen. Chromosome aberrations were induced by 43 of the chemicals, and 66 induced SCEs; 37 of the chemicals were positive for both endpoints.

Animals↗